Processing Face Encoding in Multiple Sclerosis: A fMRI Investigation (P6.134)
Article 2015 en
Authors
LV
Laura Vacchi
MR
Maria A. Rocca
GR
Gianna Carla Riccitelli
Abstract
1 min read
OBJECTIVE: We investigated behavioral and functional MRI correlates of face encoding (FE) in patients with relapse-onset multiple sclerosis (MS) and their correlation with clinico-behavioural and structural MRI measures. BACKGROUND: Encoding difficulties are among the causes of memory deficits affecting MS. No study has assessed encoding capability associated to non-verbal and social stimuli as faces in these patients. DESIGN/METHODS: Using a 3.0 Tesla scanner, a block-design episodic FE paradigm was administered to 75 MS patients (11 with clinically isolated syndromes [CIS], 40 with relapsing-remitting [RR] and 24 with secondary progressive [SP]) and 22 healthy controls (HC). A face recognition (FR) test was performed outside the scanner. Patients with abnormal performance at Paced Auditory Serial Addition Test were considered cognitively impaired. Analyses of fMRI data was performed using SPM8. T2 lesions volumes, normalized gray matter (GM) and white matter (WM) volumes were assessed and correlated with fMRI abnormalities. RESULTS: All groups activated areas involved in face perception and encoding tasks, and deactivated areas part of the default-mode network. Compared to HC and RRMS, CIS patients experienced an increased recruitment of posterior-visual areas. The thalami, para-hippocampal gyri and right anterior cingulum were more active in RRMS vs CIS and SPMS patients, while an increased recruitment of frontal areas was observed in SPMS vs RRMS. Significant correlations were found between abnormal activations and clinical, behavioral and structural MRI measures. CONCLUSIONS: Face encoding and recognition abnormalities occur in MS and vary across the different stages of the disease. Early in MS, the higher recruitment of areas typically devoted to face perception and encoding is likely to result in an adaptive response, reflecting a compensatory mechanism of cerebral reorganization. Afterwards, patients with progressive course recruit brain regions designated to higher cognitive functions, likely reflecting a maladaptive and ineffective process to cope with task-related demands.
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